Hindawi Publishing Corporation ISRN Ophthalmology Volume 2014, Article ID 481527, 6 pages http://dx.doi.org/10.1155/2014/481527
Research Article Retinopathy of Prematurity in Port Harcourt, Nigeria Adedayo O. Adio,1 Rosemary O. Ugwu,2 Chidi G. Nwokocha,1 and Augusta U. Eneh2 1 2
Department of Ophthalmology, University of Port Harcourt Teaching Hospital, Port Harcourt, Rivers State, Nigeria Department of Paediatrics, University of Port Harcourt Teaching Hospital, Rivers State, Nigeria
Correspondence should be addressed to Adedayo O. Adio; [email protected] Received 4 October 2013; Accepted 24 December 2013; Published 4 February 2014 Academic Editors: T. Mimura and Y. F. Shih Copyright © 2014 Adedayo O. Adio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Purpose. With many preterm babies now surviving as a result of improvement in neonatal care in Nigeria, the incidence of visual impairment/blindness as a result of retinopathy of prematurity (ROP) may rise. We describe our findings after screening starts for the first time in a 15-year-old special care baby unit so as to establish the incidence and risk factors for developing ROP. Methods. A prospective study carried out at the Special Care Baby Unit (SCBU) and Pediatric Outpatient Clinics of the University of Port Harcourt Teaching Hospital between January 1 and October 31, 2012. Fifty-three preterm babies (of 550 neonates admitted within the study period) delivered before 32 completed weeks and weighing less than 1500 g were included in the study following informed consent and the main outcome measure was the development of any stage of ROP. Results. Mean gestational age at birth was 28.98 ± 1.38 weeks. Mean birth weight was 1411 ± 128 g. Out of 550 babies admitted at SCBU, 87 of 100 preterms survived with 53 included in study. Twenty-five (47.2%) had different degrees of ROP with prevalence found to be 47.2%. Prevalence was higher (75%) in babies weighing 32 weeks) and higher birth weight (up to 2 kg). The incidence of ROP is known to be higher with decreasing gestational age and birth weight. The prevalence in our study was also higher than that reported in developed countries [26–28]. In developed and industrialized countries where enough financial resources allow for provision of optimum care of extremely immature newborns, adequate screening, and treatment, the rates of blindness from ROP have declined [26–28]. In contrast, in less developed countries, due to limited financing resources, the increasing survival of premature newborns is not matched by high levels of standard of care, thus resulting in increasing prevalence or the so-called third ROP epidemic [10]. The frequency and degree of the disease are inversely related to the gestational age and weight at birth. Similar was the finding in our study where the prevalence in babies weighing less than 1300 g was 75% and 58% in babies delivered
ISRN Ophthalmology Table 3: Prevalence of ROP according to birth weight and gestational age. Characteristics With ROP Without ROP Birth weight < 1300 g 6 (75%) 2 (25%) Birth weight ≥ 1300 g 19 (42%) 26 (58%) Gestational age < 30 weeks 18 (58%) 13 (42%) Gestational a ge ≥ 30 weeks 7 (32%) 15 (68%)
Total 8 (100%) 45 (100%) 31 (100%) 22 (100%)
Table 4: Stages of ROP in 25 preterm babies. Zones Zone I Zone II Zone III Total
Stage 1 0 (0%) 3 (12%) 18 (72%) 21 (84%)
Stage 2 0 (0%) 2 (8%) 1 (4%) 3 (12%)
Stage 3 1 (4%) 0 (%) 0 (0%) 1(4% )
Total 1 (4%) 5 (20%) 19(76%) 25 (100%)
before 30 weeks. Vyas et al. [29] reported an incidence of 47% in infants with birth weights between 1000 and 1251 g and 81.6% for infants weighing less than 1000 g at birth, while only 60% of infants born at 28–31 weeks developed ROP and over 80% of infants born at less than 28-week gestational age developed ROP. Other implicated risk factors are hypoxia and receiving supplemental oxygen [3, 22]. In our study also significantly more children who received supplemental oxygen developed ROP. Oxygen therapy by itself and also fluctuation in its levels have been implicated in the rapid progression of ROP in these infants and therefore constant monitoring to within levels less than 90% in their management with the minimum of pulse oximeters. Our monitoring however is up to standard protocols but still requires to be improved upon. Sepsis was significantly associated with development of any degree of ROP. This was also reported by other studies [24, 30]. In sepsis, microorganisms infiltrate vascular endothelial cells of the eyes and induce phagocytosis, endothelial cell damage, and release of proinflammatory cytokines especially endothelial growth factor which has been specifically implicated in the pathogenesis of ROP [31]. The debilitation it produces also has deleterious effect on the children inhibiting rapid weight gain the absence of which is another factor implicated in the progression of ROP. Babies that received multiple blood transfusions also developed ROP which has been identified as a risk factor for ROP in several studies [26, 32, 33]. Damaging effects on the retina through increase in free iron that may catalyze Fenton reactions, to produce free hydroxyl radicals capable of damaging the retina [32–34]. Significantly more babies delivered by caesarian section had ROP as also reported by Shah et al. [35]. While one study in contrast reported that vaginal delivery was a significant and independent predictor of threshold ROP in ELBW infants, [36] others found no relationship with the mode of delivery [26, 37] Gender and receiving phototherapy were not identified as risk factors in our study as was also reported by others [26]. In contrast, Darlow et al. [38] found the male gender a significant risk factor to development of ROP.
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Table 5: Comparison of some risk factors between preterm babies with ROP (𝑛 = 25) and preterms without evidence of ROP (𝑛 = 28). Risk factors Mean gestational age (weeks) Mean birth weight (g) Use of supplemental oxygen Presence of sepsis Apnoeic spells Phototherapy Neonatal jaundice Multiple blood transfusion Male gender Female gender Vaginal delivery Caesarian section
With ROP 28.9 1372 24 20 9 25 25 18 19 6 5 20
Without ROP 29.8 1446 7 4 4 24 26 5 12 16 21 7
𝜒2 value 0.00 0.01 6.17 7.47 1.25 0.04 0.0 5.11 1.05 1.78 4.66 4.22
𝑃 value 1.0 0.94 0.01∗ 0.006∗ 0.26 0.8 1.0 0.02∗ 0.3 0.18 0.03∗ 0.04∗
(∗ 𝑃 ≤ 0.05).
As reported in earlier ROP studies, [5, 39, 40] spontaneous resolution is seen in most (80%) cases without visual loss from retinal detachment or scars. In our study, this could be because very sick and vulnerable babies may not have survived. However, these babies will still require periodic followup despite regression as the risk of other eye conditions like myopia and strabismus is known to be increased in them [2, 9, 10].
5. Conclusion Though the prevalence of ROP in this cohort of preterm babies is high (47.2%) it did not progress to severe blinding disease; rather it spontaneously regressed and therefore the problem is actually very low. However screening identified at least one vision threatening ROP in our study. Better survival in the coming years could lead to increased epidemic of ROP blindness. Though investing in equipment for treatment may not be completely necessary at this point of time, it is important to set up screening protocols and its attendant equipment in our SCBUs to be able to identify the few who may develop vision threatening disease. Babies do not become blind as numbers but each baby becomes blind as an individual.
Conflict of Interests The authors report no conflict of interests.
Acknowledgments The authors would like to dedicate the paper to the parents of their preterm babies. The authors declare that they have full access to the details and take full responsibility for the integrity and accuracy of the data analysis. They have no financial interest. Adedayo O. Adio performed the ophthalmic examination, Rosemary O. Ugwu and Augusta U. Eneh examined the neonates and contributed pediatric references, and Chidi G. Nwokocha did most of the literature
search. Adedayo O. Adio, Chidi G. Nwokocha, and Rosemary O. Ugwu wrote the paper.
References [1] C. Gilbert and A. Foster, “Childhood blindness in the context of VISION 2020—the right to sight,” Bulletin of the World Health Organization, vol. 79, no. 3, pp. 227–232, 2001. [2] S. E. Olitsky and L. B. Nelson, “Disorders of the eyes,” in Nelson Textbook of Pediatrics, R. E. Behrman, R. M. Kliegman, and H. B. Jenson, Eds., pp. 6588–6591, WB Saunders, Philadelphia, Pa, USA, 17th edition, 2003. [3] K. Campbell, “Intensive oxygen therapy as a possible cause for retrolental fibroplasia. A clinical approach,” Medical Journal of Australia, vol. 2, pp. 48–50, 1951. [4] F. L. Kretzer and H. M. Hittner, “Retinopathy of prematurity: clinical implications of retinal development,” Archives of Disease in Childhood, vol. 63, no. 10, pp. 1151–1167, 1988. [5] The Committee for the Classification of Retinopathy of Prematurity, “An international classification of retinopathy of prematurity,” Archives of Ophthalmology, vol. 102, pp. 1130–1134, 1984. [6] A. R. Fielder, D. E. Shaw, J. Robinson, and Y. K. Ng, “Natural history of retinopathy of prematurity: a prospective study,” Eye, vol. 6, part 3, pp. 233–242, 1992. [7] J. O’Sullivan, C. Gilbert, and A. Forster, “The causes of childhood blindness in South Africa,” South African Medical Journal, vol. 87, pp. 1691–1695, 1997. [8] S. Varughese, C. Gilbert, C. Pieper, and C. Cook, “Retinopathy of prematurity in South Africa: an assessment of needs, resources and requirements for screening programmes,” British Journal of Ophthalmology, vol. 92, no. 7, pp. 879–882, 2008. [9] B. J. Kushner and S. Sondheimer, “Medical treatment of glaucoma associated with cicatricial retinopathy of prematurity,” American Journal of Ophthalmology, vol. 94, no. 3, pp. 313–317, 1982. [10] R. Clemett and B. Darlow, “Results of screening low-birthweight infants for retinopathy of prematurity,” Current Opinion in Ophthalmology, vol. 10, no. 3, pp. 155–163, 1999. [11] H. A. Ajibode, “Retinopathy of prematurity: a review,” Nigerian Journal of Paediatrics, vol. 31, no. 3, pp. 61–66, 2004.
6 [12] “Retinopathy of prematurity: guidelines for screening and treatment. The report of a joint working party of the Royal College of Opthalmologists and the British Association of Perinatal Medicine,” Early Human Development, vol. 46, no. 3, pp. 239–258, 1996. [13] B. Ackerman, E. Sherwonit, and J. Williams, “Reduced incidental light exposure: effect on the development of retinopathy of prematurity in low birth weight infants,” Pediatrics, vol. 83, no. 6, pp. 958–962, 1989. [14] K. Csak, V. Szabo, A. Szabo, and A. Vannay, “Pathogenesis and genetic basis for retinopathy of prematurity,” Frontiers in Bioscience, vol. 11, no. 1, pp. 908–920, 2006. [15] M. Adekeye, Causes of blindness in children in NE Nigeria: a blind school study [Dissertation for Masters degree in Community eye health], Department of Preventive Ophthalmology, Institute of Ophthalmology, London, UK, 1996. [16] A. M. Baiyeroju-Agbeja and F. Omokhodion, “Screening for retinopathy of prematurity,” Nigerian Journal of Ophthalmology, vol. 6, no. 1, pp. 23–25, 1998. [17] Cryotherapy for Retinopathy of Prematurity Cooperative Group, “Multicenter trial of cryotherapy for retinopathy of prematurity: preliminary results,” Archives of Ophthalmology, vol. 106, pp. 471–479, 1988. [18] L. M. S. Dubowitz, V. Dubowitz, and C. Goldberg, “Clinical assessment of gestational age in the newborn infant,” The Journal of Pediatrics, vol. 77, no. 1, pp. 1–10, 1970. [19] International Committee for the Classification of Retinopathy of Prematurity, “The international classification of retinopathy of prematurity revisited: an international committee for the classification of retinopathy of prematurity,” Archives of Ophthalmology, vol. 123, no. 7, pp. 991–999, 2005. [20] S. Jalali, R. Anand, H. Kumar, M. R. Dogra, R. Azad, and L. Gopal, “Programme planning and screening strategy in retinopathy of prematurity,” Indian Journal of Ophthalmology, vol. 51, no. 1, pp. 89–99, 2003. [21] W. V. Good, “Final results of the Early Treatment for Retinopathy of Prematurity (ETROP) randomized trial,” Transactions of the American Ophthalmological Society, vol. 102, pp. 233–250, 2004. [22] T. L. Terry, “Extreme prematurity and fibroblastic overgrowth of persistent vascular sheath behind each crystalline lens. I. Preliminary report,” American Journal of Ophthalmology, vol. 25, no. 2, pp. 203–204, 1942. [23] D. L. Phelps, “Retinopathy of prematurity: an estimate of vision loss in the United States—1979,” Pediatrics, vol. 67, no. 6, pp. 924–926, 1981. [24] A. H. A. A. Hakeem, G. B. Mohamed, and M. F. Othman, “Retinopathy of prematurity: a study of prevalence and risk factors,” Middle East African Journal of Ophthalmology, vol. 19, no. 3, pp. 289–294, 2012. [25] Y. Chen, X.-X. Li, H. Yin et al., “Risk factors for retinopathy of prematurity in six neonatal intensive care units in Beijing,” British Journal of Ophthalmology, vol. 92, no. 3, pp. 326–330, 2008. [26] N. Hussain, J. Clive, and V. Bhandari, “Current incidence of retinopathy of prematurity, 1989–1997,” Pediatrics, vol. 104, no. 3, p. e26, 1999. [27] E. Rowlands, A. C. W. Ionides, S. Chinn, H. Mackinnon, and C. C. Davey, “Reduced incidence of retinopathy of prematurity,” British Journal of Ophthalmology, vol. 85, no. 8, pp. 933–935, 2001.
ISRN Ophthalmology [28] P. M. Pennefather, W. Tin, M. P. Clarke, S. Fritz, and N. P. Strong, “Retinopathy of prematurity in a controlled trial of prophylactic surfactant treatment,” British Journal of Ophthalmology, vol. 80, no. 5, pp. 420–424, 1996. [29] J. Vyas, D. Field, E. S. Draper et al., “Severe retinopathy of prematurity and its association with different rates of survival in infants of less than 1251 g birth weight,” Archives of Disease in Childhood, vol. 82, no. 2, pp. F145–F149, 2000. [30] P.-M. Liu, P.-C. Fang, C.-B. Huang et al., “Risk factors of retinopathy of prematurity in premature infants weighing less than 1600 g,” American Journal of Perinatology, vol. 22, no. 2, pp. 115–120, 2005. [31] J. Stone, T. Chan-Ling, J. Pe’er, A. Itin, H. Gnessin, and E. Keshet, “Roles of vascular endothelial growth factor and astrocyte degeneration in the genesis of retinopathy of prematurity,” Investigative Ophthalmology and Visual Science, vol. 37, no. 2, pp. 290–299, 1996. [32] C. Clark, J. A. H. Gibbs, R. Maniello, E. W. Outerbridge, and J. V. Aranda, “Blood transfusion: a possible risk factor in retrolental fibroplasia,” Acta Paediatrica Scandinavica, vol. 70, no. 4, pp. 535–539, 1981. [33] L. M. Sacks, D. B. Schaffer, and E. K. Anday, “Retrolental fibroplasia and blood transfusion in very low-birth-weight infants,” Pediatrics, vol. 68, no. 6, pp. 770–774, 1981. [34] E. Mikaniki, M. Mikaniki, and A. H. Shirzadian, “Effects of blood transfusion on retinopathy of prematurity,” in Blood Transfusion in Clinical Practice, P. K. Kochhar, Ed., InTech, Vienna, Austria, 2012, http://www.intechopen.com/ books/blood-transfusion-in-clinicalpractice/effects-of-bloodtransfusion-on-retinopathy-of-prematurity. [35] V. A. Shah, C. L. Yeo, Y. L. F. Ling, and L. Y. Ho, “Incidence, risk factors of retinopathy of prematurity among very low birth weight infants in Singapore,” Annals of the Academy of Medicine Singapore, vol. 34, no. 2, pp. 169–178, 2005. [36] P. Manzoni, D. Farina, A. Maestri et al., “Mode of delivery and threshold retinopathy of prematurity in pre-term ELBW neonates,” Acta Paediatrica, International Journal of Paediatrics, vol. 96, no. 2, pp. 221–226, 2007. [37] V. Seiberth and O. Linderkamp, “Risk factors in retinopathy of prematurity: a multivariate statistical analysis,” Ophthalmologica, vol. 214, no. 2, pp. 131–135, 2000. [38] B. A. Darlow, J. L. Hutchinson, D. J. Henderson-Smart, D. A. Donoghue, J. M. Simpson, and N. J. Evans, “Prenatal risk factors for severe retinopathy of prematurity among very preterm infants of the Australian and New Zealand Neonatal Network,” Pediatrics, vol. 115, no. 4, pp. 990–996, 2005. [39] E. A. Palmer, J. T. Flynn, R. J. Hardy et al., “Incidence and early course of retinopathy of prematurity,” Ophthalmology, vol. 98, no. 11, pp. 1628–1640, 1991. [40] Cryotherapy for Retinopathy of Prematurity Cooperative Group, “The natural ocular outcome of premature birth and retinopathy: status at 1 year,” Archives of Ophthalmology, vol. 112, no. 7, pp. 903–912, 1994.
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Research Article Retinopathy of Prematurity in Port Harcourt, Nigeria Adedayo O. Adio,1 Rosemary O. Ugwu,2 Chidi G. Nwokocha,1 and Augusta U. Eneh2 1 2
Department of Ophthalmology, University of Port Harcourt Teaching Hospital, Port Harcourt, Rivers State, Nigeria Department of Paediatrics, University of Port Harcourt Teaching Hospital, Rivers State, Nigeria
Correspondence should be addressed to Adedayo O. Adio; [email protected] Received 4 October 2013; Accepted 24 December 2013; Published 4 February 2014 Academic Editors: T. Mimura and Y. F. Shih Copyright © 2014 Adedayo O. Adio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Purpose. With many preterm babies now surviving as a result of improvement in neonatal care in Nigeria, the incidence of visual impairment/blindness as a result of retinopathy of prematurity (ROP) may rise. We describe our findings after screening starts for the first time in a 15-year-old special care baby unit so as to establish the incidence and risk factors for developing ROP. Methods. A prospective study carried out at the Special Care Baby Unit (SCBU) and Pediatric Outpatient Clinics of the University of Port Harcourt Teaching Hospital between January 1 and October 31, 2012. Fifty-three preterm babies (of 550 neonates admitted within the study period) delivered before 32 completed weeks and weighing less than 1500 g were included in the study following informed consent and the main outcome measure was the development of any stage of ROP. Results. Mean gestational age at birth was 28.98 ± 1.38 weeks. Mean birth weight was 1411 ± 128 g. Out of 550 babies admitted at SCBU, 87 of 100 preterms survived with 53 included in study. Twenty-five (47.2%) had different degrees of ROP with prevalence found to be 47.2%. Prevalence was higher (75%) in babies weighing 32 weeks) and higher birth weight (up to 2 kg). The incidence of ROP is known to be higher with decreasing gestational age and birth weight. The prevalence in our study was also higher than that reported in developed countries [26–28]. In developed and industrialized countries where enough financial resources allow for provision of optimum care of extremely immature newborns, adequate screening, and treatment, the rates of blindness from ROP have declined [26–28]. In contrast, in less developed countries, due to limited financing resources, the increasing survival of premature newborns is not matched by high levels of standard of care, thus resulting in increasing prevalence or the so-called third ROP epidemic [10]. The frequency and degree of the disease are inversely related to the gestational age and weight at birth. Similar was the finding in our study where the prevalence in babies weighing less than 1300 g was 75% and 58% in babies delivered
ISRN Ophthalmology Table 3: Prevalence of ROP according to birth weight and gestational age. Characteristics With ROP Without ROP Birth weight < 1300 g 6 (75%) 2 (25%) Birth weight ≥ 1300 g 19 (42%) 26 (58%) Gestational age < 30 weeks 18 (58%) 13 (42%) Gestational a ge ≥ 30 weeks 7 (32%) 15 (68%)
Total 8 (100%) 45 (100%) 31 (100%) 22 (100%)
Table 4: Stages of ROP in 25 preterm babies. Zones Zone I Zone II Zone III Total
Stage 1 0 (0%) 3 (12%) 18 (72%) 21 (84%)
Stage 2 0 (0%) 2 (8%) 1 (4%) 3 (12%)
Stage 3 1 (4%) 0 (%) 0 (0%) 1(4% )
Total 1 (4%) 5 (20%) 19(76%) 25 (100%)
before 30 weeks. Vyas et al. [29] reported an incidence of 47% in infants with birth weights between 1000 and 1251 g and 81.6% for infants weighing less than 1000 g at birth, while only 60% of infants born at 28–31 weeks developed ROP and over 80% of infants born at less than 28-week gestational age developed ROP. Other implicated risk factors are hypoxia and receiving supplemental oxygen [3, 22]. In our study also significantly more children who received supplemental oxygen developed ROP. Oxygen therapy by itself and also fluctuation in its levels have been implicated in the rapid progression of ROP in these infants and therefore constant monitoring to within levels less than 90% in their management with the minimum of pulse oximeters. Our monitoring however is up to standard protocols but still requires to be improved upon. Sepsis was significantly associated with development of any degree of ROP. This was also reported by other studies [24, 30]. In sepsis, microorganisms infiltrate vascular endothelial cells of the eyes and induce phagocytosis, endothelial cell damage, and release of proinflammatory cytokines especially endothelial growth factor which has been specifically implicated in the pathogenesis of ROP [31]. The debilitation it produces also has deleterious effect on the children inhibiting rapid weight gain the absence of which is another factor implicated in the progression of ROP. Babies that received multiple blood transfusions also developed ROP which has been identified as a risk factor for ROP in several studies [26, 32, 33]. Damaging effects on the retina through increase in free iron that may catalyze Fenton reactions, to produce free hydroxyl radicals capable of damaging the retina [32–34]. Significantly more babies delivered by caesarian section had ROP as also reported by Shah et al. [35]. While one study in contrast reported that vaginal delivery was a significant and independent predictor of threshold ROP in ELBW infants, [36] others found no relationship with the mode of delivery [26, 37] Gender and receiving phototherapy were not identified as risk factors in our study as was also reported by others [26]. In contrast, Darlow et al. [38] found the male gender a significant risk factor to development of ROP.
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Table 5: Comparison of some risk factors between preterm babies with ROP (𝑛 = 25) and preterms without evidence of ROP (𝑛 = 28). Risk factors Mean gestational age (weeks) Mean birth weight (g) Use of supplemental oxygen Presence of sepsis Apnoeic spells Phototherapy Neonatal jaundice Multiple blood transfusion Male gender Female gender Vaginal delivery Caesarian section
With ROP 28.9 1372 24 20 9 25 25 18 19 6 5 20
Without ROP 29.8 1446 7 4 4 24 26 5 12 16 21 7
𝜒2 value 0.00 0.01 6.17 7.47 1.25 0.04 0.0 5.11 1.05 1.78 4.66 4.22
𝑃 value 1.0 0.94 0.01∗ 0.006∗ 0.26 0.8 1.0 0.02∗ 0.3 0.18 0.03∗ 0.04∗
(∗ 𝑃 ≤ 0.05).
As reported in earlier ROP studies, [5, 39, 40] spontaneous resolution is seen in most (80%) cases without visual loss from retinal detachment or scars. In our study, this could be because very sick and vulnerable babies may not have survived. However, these babies will still require periodic followup despite regression as the risk of other eye conditions like myopia and strabismus is known to be increased in them [2, 9, 10].
5. Conclusion Though the prevalence of ROP in this cohort of preterm babies is high (47.2%) it did not progress to severe blinding disease; rather it spontaneously regressed and therefore the problem is actually very low. However screening identified at least one vision threatening ROP in our study. Better survival in the coming years could lead to increased epidemic of ROP blindness. Though investing in equipment for treatment may not be completely necessary at this point of time, it is important to set up screening protocols and its attendant equipment in our SCBUs to be able to identify the few who may develop vision threatening disease. Babies do not become blind as numbers but each baby becomes blind as an individual.
Conflict of Interests The authors report no conflict of interests.
Acknowledgments The authors would like to dedicate the paper to the parents of their preterm babies. The authors declare that they have full access to the details and take full responsibility for the integrity and accuracy of the data analysis. They have no financial interest. Adedayo O. Adio performed the ophthalmic examination, Rosemary O. Ugwu and Augusta U. Eneh examined the neonates and contributed pediatric references, and Chidi G. Nwokocha did most of the literature
search. Adedayo O. Adio, Chidi G. Nwokocha, and Rosemary O. Ugwu wrote the paper.
References [1] C. Gilbert and A. Foster, “Childhood blindness in the context of VISION 2020—the right to sight,” Bulletin of the World Health Organization, vol. 79, no. 3, pp. 227–232, 2001. [2] S. E. Olitsky and L. B. Nelson, “Disorders of the eyes,” in Nelson Textbook of Pediatrics, R. E. Behrman, R. M. Kliegman, and H. B. Jenson, Eds., pp. 6588–6591, WB Saunders, Philadelphia, Pa, USA, 17th edition, 2003. [3] K. Campbell, “Intensive oxygen therapy as a possible cause for retrolental fibroplasia. A clinical approach,” Medical Journal of Australia, vol. 2, pp. 48–50, 1951. [4] F. L. Kretzer and H. M. Hittner, “Retinopathy of prematurity: clinical implications of retinal development,” Archives of Disease in Childhood, vol. 63, no. 10, pp. 1151–1167, 1988. [5] The Committee for the Classification of Retinopathy of Prematurity, “An international classification of retinopathy of prematurity,” Archives of Ophthalmology, vol. 102, pp. 1130–1134, 1984. [6] A. R. Fielder, D. E. Shaw, J. Robinson, and Y. K. Ng, “Natural history of retinopathy of prematurity: a prospective study,” Eye, vol. 6, part 3, pp. 233–242, 1992. [7] J. O’Sullivan, C. Gilbert, and A. Forster, “The causes of childhood blindness in South Africa,” South African Medical Journal, vol. 87, pp. 1691–1695, 1997. [8] S. Varughese, C. Gilbert, C. Pieper, and C. Cook, “Retinopathy of prematurity in South Africa: an assessment of needs, resources and requirements for screening programmes,” British Journal of Ophthalmology, vol. 92, no. 7, pp. 879–882, 2008. [9] B. J. Kushner and S. Sondheimer, “Medical treatment of glaucoma associated with cicatricial retinopathy of prematurity,” American Journal of Ophthalmology, vol. 94, no. 3, pp. 313–317, 1982. [10] R. Clemett and B. Darlow, “Results of screening low-birthweight infants for retinopathy of prematurity,” Current Opinion in Ophthalmology, vol. 10, no. 3, pp. 155–163, 1999. [11] H. A. Ajibode, “Retinopathy of prematurity: a review,” Nigerian Journal of Paediatrics, vol. 31, no. 3, pp. 61–66, 2004.
6 [12] “Retinopathy of prematurity: guidelines for screening and treatment. The report of a joint working party of the Royal College of Opthalmologists and the British Association of Perinatal Medicine,” Early Human Development, vol. 46, no. 3, pp. 239–258, 1996. [13] B. Ackerman, E. Sherwonit, and J. Williams, “Reduced incidental light exposure: effect on the development of retinopathy of prematurity in low birth weight infants,” Pediatrics, vol. 83, no. 6, pp. 958–962, 1989. [14] K. Csak, V. Szabo, A. Szabo, and A. Vannay, “Pathogenesis and genetic basis for retinopathy of prematurity,” Frontiers in Bioscience, vol. 11, no. 1, pp. 908–920, 2006. [15] M. Adekeye, Causes of blindness in children in NE Nigeria: a blind school study [Dissertation for Masters degree in Community eye health], Department of Preventive Ophthalmology, Institute of Ophthalmology, London, UK, 1996. [16] A. M. Baiyeroju-Agbeja and F. Omokhodion, “Screening for retinopathy of prematurity,” Nigerian Journal of Ophthalmology, vol. 6, no. 1, pp. 23–25, 1998. [17] Cryotherapy for Retinopathy of Prematurity Cooperative Group, “Multicenter trial of cryotherapy for retinopathy of prematurity: preliminary results,” Archives of Ophthalmology, vol. 106, pp. 471–479, 1988. [18] L. M. S. Dubowitz, V. Dubowitz, and C. Goldberg, “Clinical assessment of gestational age in the newborn infant,” The Journal of Pediatrics, vol. 77, no. 1, pp. 1–10, 1970. [19] International Committee for the Classification of Retinopathy of Prematurity, “The international classification of retinopathy of prematurity revisited: an international committee for the classification of retinopathy of prematurity,” Archives of Ophthalmology, vol. 123, no. 7, pp. 991–999, 2005. [20] S. Jalali, R. Anand, H. Kumar, M. R. Dogra, R. Azad, and L. Gopal, “Programme planning and screening strategy in retinopathy of prematurity,” Indian Journal of Ophthalmology, vol. 51, no. 1, pp. 89–99, 2003. [21] W. V. Good, “Final results of the Early Treatment for Retinopathy of Prematurity (ETROP) randomized trial,” Transactions of the American Ophthalmological Society, vol. 102, pp. 233–250, 2004. [22] T. L. Terry, “Extreme prematurity and fibroblastic overgrowth of persistent vascular sheath behind each crystalline lens. I. Preliminary report,” American Journal of Ophthalmology, vol. 25, no. 2, pp. 203–204, 1942. [23] D. L. Phelps, “Retinopathy of prematurity: an estimate of vision loss in the United States—1979,” Pediatrics, vol. 67, no. 6, pp. 924–926, 1981. [24] A. H. A. A. Hakeem, G. B. Mohamed, and M. F. Othman, “Retinopathy of prematurity: a study of prevalence and risk factors,” Middle East African Journal of Ophthalmology, vol. 19, no. 3, pp. 289–294, 2012. [25] Y. Chen, X.-X. Li, H. Yin et al., “Risk factors for retinopathy of prematurity in six neonatal intensive care units in Beijing,” British Journal of Ophthalmology, vol. 92, no. 3, pp. 326–330, 2008. [26] N. Hussain, J. Clive, and V. Bhandari, “Current incidence of retinopathy of prematurity, 1989–1997,” Pediatrics, vol. 104, no. 3, p. e26, 1999. [27] E. Rowlands, A. C. W. Ionides, S. Chinn, H. Mackinnon, and C. C. Davey, “Reduced incidence of retinopathy of prematurity,” British Journal of Ophthalmology, vol. 85, no. 8, pp. 933–935, 2001.
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